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Prepublished online as a Blood First Edition Paper on August 1, 2002; DOI 10.1182/blood-2002-04-1131.

Submitted April 15, 2002
Accepted July 25, 2002
Ribosomal protein S19 (RPS19) expression during erythroid differentiation
Lydie M Da Costa*, Goutham Narla, Thiebaut-Noel Willig, Luanne L Peters, Marilyn Parra, Jason Fixler, Gil Tchernia, and Mohandas Narla
Life Science Division, Lawrence Berkeley National Laboratory, Berkeley, CA, USA
Liver Disease Division, Mount Sinai Medical Center, New York, NY, USA
The Jackson Laboratory, Bar Harbor, ME, USA
Laboratoire d'Hematologie, INSERM Unite 473, Hopital le Kremlin-Bicetre, AP-HP, faculte de medecine Paris XI, Le Kremlin Bicetre, Region Paris-Ile de France, France
Red Cell Physiology Laboratory, New York Blood Center, New York, NY, USA
* Corresponding author; email: ldacosta{at}lbl.gov.
The gene encoding ribosomal protein S19 (RPS19) has been shown to be mutated in 25% of the patients affected by Diamond Blackfan Anemia (DBA), a congenital erythroblastopenia. As the role of RPS19 in erythropoiesis is still to be defined, we performed studies on RPS19 expression during terminal erythroid differentiation. Comparative analysis of the genomic sequences of human and mouse RPS19 genes enabled the identification of four conserved sequence elements in the 5' region. Characterization of transcriptional elements allowed the identification of the promoter in human RPS19 gene and the localization of a strong regulatory element in the third conserved sequence element. By Northern blot and Western blot analysis of murine splenic erythroblasts infected with the anemia inducing strain Friend virus (FAV cells), RPS19 mRNA and protein expression was shown to decrease during terminal erythroid differentiation. We anticipate that these findings will contribute to further development of our understanding of the contribution of RPS19 to erythropoiesis.

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